GIS partial discharge data enhancement method based on self attention mechanism VAE-GAN

The reliability of gas-insulated switchgear(GIS)partial discharge fault diagnosis is crucial for the safe and stable operation of power grids.This study proposed a data enhancement method based on a self-attention mechanism to optimize the VAE-GAN method and solve the problem of the lack of partial discharge samples and the unbalanced distribution between different defects.First,the non-subsampled contourlet transform(NSCT)algorithm was used to fuse the UHF and optical partial discharge signals to obtain a photoelectric fusion phase resolved partial discharge(PRPD)spectrum with richer information.Subsequently,the VAE structure was introduced into the traditional GAN,and the excellent hidden layer feature extraction ability of the VAE was used to guide the generation of the GAN.Then,the self-attention mechanism was integrated into the VAE-GAN,and the Wasserstein distance and gradient penalty mechanisms were used to optimize the network loss function and expand the sample sets to an equilibrium state.Finally,the KAZE and polar coordinate distribution entropy methods were used to extract the expanded samples.The eigenvectors of the sets were substituted into the long short-term memory(LSTM)network for partial discharge fault diagnosis.The experimental results show that the sample generation quality and fault diagnosis results of this method were significantly better than the traditional data enhancement method.The structure similarity index measure(SSIM)index is increased by 4.5%and 21.7%,respectively,and the average accuracy of fault diagnosis is increased by 22.9%,9%,5.7%,and 6.5%,respectively.The data enhancement method proposed in this study can provide a reference for GIS partial discharge fault diagnosis.

Glutamine mitigates murine burn sepsis by supporting macrophage M2 polarization through repressing the SIRT5-mediated desuccinylation of pyruvate dehydrogenase

Background:Alternative(M2)-activated macrophages drive the anti-inflammatory response against sepsis,a leading cause of death in patients suffering from burn injury.Macrophage M2 polarization is intrinsically linked with dominant oxidative phosphorylation(OXPHOS).Glutamine serves as a major anaplerotic source to fuel OXPHOS,but it remains unknown whether glutamine can modulate metabolic checkpoints in OXPHOS that favour M2 polarization.The study aims to explore whether glutamine essentially supports M2 polarization in IL-4-stimulated murine macrophages by sustaining the activity of PDH and whether glutamine augments macrophage M2 polarization and thus alleviates inflammation and organ injury in a murine burn sepsis model.Methods:To understand how glutamine promotes M2 activation in interleukin(IL-4)-treated murine macrophages,we detected glutamine-dependent M2 polarization and its relationship with the pyruvate dehydrogenase(PDH)complex by RT-PCR,flow cytometry and western blot.To explore how glutamine modulates PDH activity and thus supports M2 polarization,we compared the expression,phosphorylation and succinylation status of PDHA1 and then examined sirtuin SIRT5-dependent desuccinylation of PDHA1 and the effects of SIRT5 overexpression on M2 polarization by RT-PCR,flow cytometry and western blot.To determine whether glutamine or its metabolites affect M2 polarization,macrophages were cocultured with metabolic inhibitors,and then SIRT5 expression and M2 phenotype markers were examined by RT-PCR,flow cytometry and western blot.Finally,to confirm the in vivo effect of glutamine,we established a burn sepsis model by injecting Pseudomonas aeruginosa into burn wounds and observing whether glutamine alleviated proinflammatory injuries by RT-PCR,flow cytometry,western blot,immunofluorescent staining,hematoxylin-eosin staining and enzyme-linked immuno sorbent assay.Results:We showed that consumption of glutamine supported M2 activation in IL-4-treated murine macrophages by upregulating the activity of PDH.Mechanistically,glutamine did not affect the expression or alter the phosphorylation status of PDHA1 but instead downregulated the expression of SIRT5 and repressed SIRT5-dependent desuccinylation on PDHA1,which in turn recovered PDH activity and supported M2 polarization.This effect was implemented by its secondary metaboliteα-ketoglutarate(αKG)rather than glutamine itself.Finally,we demonstrated that glutamine pro-moted macrophage M2 polarization in a murine burn sepsis model,thereby repressing excessive inflammation and alleviating organ injury in model mice.Conclusions:Glutamine mitigates murine burn sepsis by essentially supporting macrophage M2 polarization,with a mechanism involving the repression of the SIRT5-mediated desuccinylation of pyruvate dehydrogenase that replenishes OXPHOS and sustains M2 macrophages.

PSA controls hepatic lipid metabolism by regulating the NRF2 signaling pathway

The activity of proteinase is reported to correlate with the development and progression of nonalcoholic fatty liver disease(NAFLD).Puromycin-sensitive aminopeptidase(PSA/NPEPPS)is an integral nontransmembrane enzyme that functions to catalyze the cleavage of amino acids near the N-terminus of polypeptides.A previous study suggested that this enzyme acts as a regulator of neuropeptide activity;however,the metabolic function of this enzyme in the liver has not been explored.Here,we identified the novel role of PSA in hepatic lipid metabolism.Specifically,PSA expression was lower in fatty livers from NAFLD patients and mice(HFD,ob/ob,and db/db).PSA knockdown in cultured hepatocytes exacerbated diet-induced triglyceride accumulation through enhanced lipogenesis and attenuated fatty acid β-oxidation.Moreover,PSA mediated activation of the master regulator of antioxidant response,nuclear factor erythroid 2-related factor 2(NRF2),by stabilizing NRF2 protein expression,which further induced downstream antioxidant enzymes to protect the liver from oxidative stress and lipid overload.Accordingly,liver-specific PSA overexpression attenuated hepatic lipid accumulation and steatosis in ob/ob mice.Furthermore,in human liver tissue samples,decreased PSA expression correlated with the progression of NAFLD.Overall,our findings suggest that PSA is a pivotal regulator of hepatic lipid metabolism and its antioxidant function occurs by suppressing NRF2 ubiquitination.Moreover,PSA may be a potential biomarker and therapeutic target for treating NAFLD.

Primal dual interior point dynamic programming for coordinated charging of electric vehicles

Coordinated charging of electric vehicles(EVs)is critical to provide safe and cost effective operation of distribution systems where household single phase charging of EV could contribute to imbalance of the distribution system.To date,reported researches on optimization methods for coordinated charging aiming at minimizing power losses have the disadvantages of low calculation efficiency when applied to large systems or have not taken the voltage constraints into account.The phase component and polar coordinates power flow equations of an unbalanced distribution system are derived.Primal dual interior point dynamic programming is introduced for coordinated charging of EVs to minimize distribution system losses where charging demand,voltage and current constraints have been taken into account.The proposed optimization is evaluated using an actual 423-bus case as the test system.Results are promisingwith the proposed method having good convergence under time-efficient calculations while providing optimization of power losses,lower load variance,and improvement of voltage profile versus uncoordinated scenarios.